Target：eIF2Bδ

Fields：Herpes simplex virus 1 infection

Gene Name：EIF2B4

Protein Name：Translation initiation factor eIF-2B subunit delta

Human Gene Id：8890

Human Swiss Prot No：Q9UI10

Mouse Gene Id：13667

Mouse Swiss Prot No：Q61749

Rat Gene Id：117019

Rat Swiss Prot No：Q63186

Immunogen：The antiserum was produced against synthesized peptide derived from human EIF2B4. AA range:226-275

Specificity：eIF2Bδ Polyclonal Antibody detects endogenous levels of eIF2Bδ protein.

Formulation：Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

Source：Polyclonal, Rabbit,IgG

Dilution：WB 1:500 - 1:2000. ELISA: 1:5000. Not yet tested in other applications.

Purification：The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

Concentration：1 mg/ml

Storage Stability：-15°C to -25°C/1 year(Do not lower than -25°C)

Other Name：EIF2B4;EIF2BD;Translation initiation factor eIF-2B subunit delta;eIF-2B GDP-GTP exchange factor subunit delta

Observed Band(KD)：57kD

Background： Eukaryotic initiation factor 2B (EIF2B), which is necessary for protein synthesis, is a GTP exchange factor composed of five different subunits. The protein encoded by this gene is the fourth, or delta, subunit. Defects in this gene are a cause of leukoencephalopathy with vanishing white matter (VWM) and ovarioleukodystrophy. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008],

Function：disease:Defects in EIF2B4 are a cause of leukodystrophy with vanishing white matter (VWM) [MIM:603896]. VWM is a leukodystrophy that occurs mainly in children. Neurological signs include progressive cerebellar ataxia, spasticity, inconstant optic atrophy and relatively preserved mental abilities. The disease is chronic-progressive with, in most individuals, additional episodes of rapid deterioration following febrile infections or minor head trauma. While childhood onset is the most common form of the disorder, some severe forms are apparent at birth. A severe, early-onset form seen among the Cree and Chippewayan populations of Quebec and Manitoba is called Cree leukoencephalopathy. Milder forms may not become evident until adolescence or adulthood. Some females with milder forms of the disease who survive to adolescence exhibit ovarian dysfunction. This variant of the disorder is called

Subcellular Location：cytoplasm,cytosol,eukaryotic translation initiation factor 2B complex,

Expression： Adrenal gland,Brain,Lung,Testis,Uterus,